Role of superoxide and thromboxane receptors in acute angiotensin II-induced vasoconstriction of rabbit vessels

Pfister, Sandra L.; Nithipatikom, Kasem; Campbell, William B.

doi:10.1152/ajpheart.01135.2010

Cited by 13 publications

(13 citation statements)

References 37 publications

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“…Although the renin-angiotensin system has been implicated in age-dependent impaired endothelium-dependent relaxation [5, 10] and despite the fact that aging substantially increases Ang II-mediated concentrations in the aorta from nonhuman primates [8], we unexpectedly observed that in carotid arteries, Ang II-induced contractions as well as gene expression of the two isoforms of the rodent AT 1 receptor that mediate constrictor effects of Ang II, AT 1A and AT 1B [5], remain unaffected by aging. Unlike other vascular beds [5, 10, 47, 48], responses of the common carotid artery to Ang II were also independent of functional NADPH oxidase and TP receptor signaling, suggesting that Ang II-dependent regulation of carotid artery tone in mice is maintained even at advanced age. The tachyphylaxis of the weak responses to Ang II poses a limitation to the current study since it did not allow study of the arteries’ sensitivity to Ang II.…”

Section: Discussionmentioning

confidence: 94%

Endothelin-1 but not angiotensin II contributes to functional aging in murine carotid arteries

et al. 2014

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Aims Aging is a major risk factor for carotid artery disease and stroke. Endothelin-1 (ET-1) and angiotensin II (Ang II) are important modifiers of vascular disease, partly through increased activity of NADPH oxidase and vasoconstrictor prostanoids. Since the renin-angiotensin and endothelin systems become activated with age, we hypothesized that aging affects NADPH oxidase- and prostanoid-dependent contractions to ET-1 and Ang II. Methods Carotid artery rings of young (4 month-old) and old (24 month-old) C57BL6 mice were pretreated with the NO synthase inhibitor L-NAME to exclude differential effects of NO. Contractions to ET-1 and Ang II were determined in the presence and absence of NADPH oxidase (gp91ds-tat) or thromboxane-prostanoid receptor (SQ 29,548) inhibition. Gene expression of endothelin and angiotensin receptors was measured by qPCR. Key findings Aging reduced ET-1-induced contractions and diminished ETA but increased ETB receptor gene expression levels. Gp91ds-tat inhibited contractions to ET-1 in young and to a greater extent old animals, whereas SQ 29,548 had no effect. Ang II-induced contractions were weak compared to ET-1 and unaffected by aging, gp91ds-tat, and SQ 29,548. Aging had also no effect on AT1A and AT1B receptor gene expression levels. Significance Aging in carotid arteries decreases ETA receptor gene expression and responsiveness to ET-1, which nevertheless becomes increasingly dependent upon NAPDH oxidase activity with age; responses to Ang II and gene expression of its receptors are however unaffected. These findings suggest that physiological aging differentially regulates functional responses to G protein-coupled receptor agonists and the signaling pathways associated with their activation.

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Section: Discussionmentioning

confidence: 94%

Endothelin-1 but not angiotensin II contributes to functional aging in murine carotid arteries

et al. 2014

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“…, Pfister et al . ). Quenching of

O_{2}^{• -}

with PEG‐SOD blunted AngII reactivity similarly in SS‐13 BN rats on normal diet and hypercaloric diet, whereas H 2 O 2 ‐mediated AngII reactivity was only present in aortas from SS‐13 BN rats on hypercaloric diet.…”

Section: Discussionmentioning

confidence: 97%

“…It is well-known that in the blood vessel wall AngII is a potent stimulator of ROS including O À 2 (Berry et al 2000) and H 2 O 2 (Zafari et al 1998). Both of these ROS are known to mediate AngII-induced vasoconstriction (Kawazoe et al 1999, Torrecillas et al 2001, Shastri et al 2002, de Groot et al 2004, Puntmann et al 2005, Hussain et al 2006, Bagi et al 2008, Kim et al 2010, Pfister et al 2011. Quenching of O À 2 with PEG-SOD blunted AngII reactivity similarly in SS-13 BN rats on normal diet and hypercaloric diet, whereas H 2 O 2 -mediated AngII reactivity was only present in aortas from SS-13 BN rats on hypercaloric diet.…”

Section: Discussionmentioning

confidence: 98%

Short‐term hypercaloric diet induces blunted aortic vasoconstriction and enhanced vasorelaxation via increased nitric oxide synthase 3 activity and expression in Dahl salt‐sensitive rats

2012

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Aim To test the hypothesis that hyper-caloric diet on mechanisms of angiotensin (Ang)II-induced vasoconstriction in Dahl salt-sensitive (SS) rats and genetic control SS-13BN rats. Methods Aortic function was assessed using wire myography in 16-week-old rats maintained on a normal diet or started on a 4-week hyper-caloric diet at 12-weeks-old. Results On normal diet, AngII vasoconstriction was greater in SS rats than SS-13BN rats. Intriguingly, the AngII response was reduced in aortic rings from SS rats on hyper-caloric diet versus normal diet, whereas this response was not altered by hyper-caloric diet in SS-13BN rats. We probed whether O2−, H2O2, or NO mediate the AngII response. PEG-SOD reduced the AngII response in all 4 groups. Catalase treatment of aortic rings did not alter aortic AngII response from SS rats on hyper-caloric but reduced the aortic AngII response of SS rats on normal diet; the exact opposite finding was observed with catalase in SS-13BN rats. L-NAME increased AngII response in SS rats on hyper-caloric but was without effect in the normal diet group. In stark contrast, L-NAME did not alter the AngII response in SS-13BN rats on hyper-caloric diet, yet L-NAME enhanced AngII responsiveness in the normal diet group. In SS rats, hyper-caloric diet increased aortic NOS3 activity and expression corresponding with increased endothelial-dependent vasorelaxation. Conclusion A short-term hyper-caloric diet elicits a vasodilatory phenotype in SS rats, but not in SS-13BN rats, by increasing NOS3 expression and function as well as reducing H2O2 function.

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“…It is noteworthy that lungs and kidneys are among the most affected extrapancreatic tissues in severe acute pancreatitis. In addition, isoprostanes induced vasoconstriction of human radial artery and contraction of vascular smooth muscle from porcine carotid artery via thromboxane A 2 receptors [53], [54], and seem to be involved in angiotensin II-induced vasoconstriction in rabbit aorta or mesentery artery [55]. Furthermore, high isoprostane levels are considered an independent risk factor for coronary heart disease [33].…”

Section: Discussionmentioning

confidence: 99%

Obese Rats Exhibit High Levels of Fat Necrosis and Isoprostanes in Taurocholate-Induced Acute Pancreatitis

et al. 2012

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BackgroundObesity is a prognostic factor for severity in acute pancreatitis in humans. Our aim was to assess the role of oxidative stress and abdominal fat in the increased severity of acute pancreatitis in obese rats.MethodologyTaurocholate-induced acute pancreatitis was performed in lean and obese Zucker rats. Levels of reduced glutathione, oxidized glutathione, L-cysteine, cystine, and S-adenosylmethionine were measured in pancreas as well as the activities of serine/threonine protein phosphatases PP1 and PP2A and tyrosin phosphatases. Isoprostane, malondialdehyde, triglyceride, and free fatty acid levels and lipase activity were measured in plasma and ascites. Lipase activity was measured in white adipose tissue with and without necrosis and confirmed by western blotting.FindingsUnder basal conditions obese rats exhibited lower reduced glutathione levels in pancreas and higher triglyceride and free fatty acid levels in plasma than lean rats. S-adenosyl methionine levels were markedly increased in pancreas of obese rats. Acute pancreatitis in obese rats led to glutathione oxidation and lower reduced glutathione levels in pancreas together with decreased activities of redox-sensitive phosphatases PP1, and PP2A. S-adenosyl methionine levels decreased but cystine levels increased markedly in pancreas upon pancreatitis. Acute pancreatitis triggered an increase in isoprostane levels in plasma and ascites in obese rats. Free fatty acid levels were extremely high in pancreatitis-associated ascitic fluid from obese rats and lipase was bound with great affinity to white adipose tissue, especially to areas of necrosis.ConclusionsOur results show that oxidative stress occurs locally and systemically in obese rats with pancreatitis favouring inactivation of protein phosphatases in pancreas, which would promote up-regulation of pro-inflammatory cytokines, and the increase of isoprostanes which might cause powerful pulmonary and renal vasoconstriction. Future studies are needed to confirm the translational relevance of the present findings obtained in a rat model of taurocholate-induced pancreatic damage and necrosis.

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Role of superoxide and thromboxane receptors in acute angiotensin II-induced vasoconstriction of rabbit vessels

Cited by 13 publications

References 37 publications

Endothelin-1 but not angiotensin II contributes to functional aging in murine carotid arteries

Endothelin-1 but not angiotensin II contributes to functional aging in murine carotid arteries

Short‐term hypercaloric diet induces blunted aortic vasoconstriction and enhanced vasorelaxation via increased nitric oxide synthase 3 activity and expression in Dahl salt‐sensitive rats

Obese Rats Exhibit High Levels of Fat Necrosis and Isoprostanes in Taurocholate-Induced Acute Pancreatitis

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